The present invention generally relates to a method, a device and a computer program for generating a control signal for a cochlear implant based on an audio signal, in particular, to a concept for selective generation of electrical stimuli for cochlear implants by means of a two-stage back-filtration of a neurotransmitter vesicle release distribution.
For a long time, it has been a goal in medicine and medical technologies in particular to enable people suffering from a hearing disorder to take part in normal social life with as little impairments as possible. Conventional hearing aids amplifying a received acoustic signal, and, thus, enabling patients hard of hearing to perceive acoustic signals of low loudness have already been in existence for many years.
For some years, it has been even possible to help patients with a serious and non-recoverable damage to the inner ear at least to a limited auditory sensation. For this purpose, the patient's intact auditory nerves are excited by means of electrodes of a cochlear implant. In this context, the corresponding excitation signals are derived from an audio signal which is to be returned to the patient concerned.
Furthermore, a neurophysiologically-parametrized auditory computer simulation model is known, which is described, for example, in the publication “Neuronale Repräsentation des Hörvorgangs als Basis” (Neuronal Representation of the Auditory Process as a Basis) by G. Szepannek, F. Klefenz and C. Weihs (Informatik-Spektrum, vol. 28, no. 5, pp. 389-395, October 2005, Springer).
A hydromechanical liquid column excitation in the cochlea and a traveling wave motion on the basilar membrane are modeled by a set of coupled electromechanical differential equations. Detailed explanations concerning this topic may be found, for example, in the PhD thesis “Ein psychophysiologisches Gehörmodell zur Nachbildung von Wahrnehmungsschwellen für die Audiocodierung” (A Psychophysiological Auditory Model for Replication of Perception Thresholds for Audio Coding) by F. Baumgarte (PhD thesis at the University of Hannover, 2000).
The motion, or traveling wave motion, of the basilar membrane leads to a coupling motion of the stereocilia of the inner hair cells. A deflection of the stereocilia from their rest position depolarizes a rest membrane voltage of the inner hair cell, whereby a probability of an exit of a neurotransmitter vesicle from the hair cell into the synaptic cleft is increased. Exit times of the neurotransmitter vesicles are modeled according to a model by Meddis-Poveda. Modeling the voltage shape in nerve cells is based on a work by Hodgkin and Huxley. In this context, membrane voltage is influenced by ion exchange as well as an external current through the released neurotransmitters. If a vesicle diffuses from the presynaptic inner hair cell (IHC) into a synaptic cleft, it will bond to a receptor protein of the post-synaptic membrane and release charge. By the molecules of a vesicle, the postsynaptic potential increases approximately by 0.5 to 1 mV. If the polarization of the postsynaptic nerve cell exceeds a particular threshold value ν, an action potential is released.
Action potentials are characterized by their almost approximately identical course. Initially, the membrane voltage extremely strongly depolarizes for a very short duration of less than 1 ms, subsequently, it hyperpolarizes and is blocked for a period of time in which no further action potentials can occur.